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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Ataxia telangiectasia mutated homolog

serine/threonine protein kinase; critical regulator of the cellular DNA damage response [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: p53, CAN, V1a, HAD, p21
Papers on Atm
Low-dose irradiation prior to bone marrow transplantation results in ATM activation and increased lethality in Atm-deficient mice.
Schubert et al., Frankfurt am Main, Germany. In Bone Marrow Transplant, Feb 2016
Repopulation with ATM-competent bone marrow-derived cells (BMDCs) significantly prolonged the lifespan and improved the phenotype of Atm-deficient mice.
Alteration in 5-hydroxymethylcytosine-mediated epigenetic regulation leads to Purkinje cell vulnerability in ATM deficiency.
Li et al., Kunming, China. In Brain, Dec 2015
A long-standing mystery surrounding ataxia-telangiectasia is why it is mainly cerebellar neurons, Purkinje cells in particular, that appear vulnerable to ATM deficiency.
Microsatellite instability detected in tumor-related genes in C57BL/6J mice with thymic lymphoma induced by N-methyl-N-nitrosourea.
Chen et al., Beijing, China. In Mutat Res, Dec 2015
MSI loci in intronic regions of Atm, Msh6 and p21 and MSI in the 3'UTR of Pms2 were detected in MNU-treated mice.
Defining ATM-independent Functions of the Mre11 Complex with a Novel Mouse Model.
Petrini et al., Kettering, United States. In Mol Cancer Res, Dec 2015
UNASSIGNED: The Mre11 complex (Mre11, Rad50 and Nbs1) occupies a central node of the DNA damage response (DDR) network, and is required for ATM activation in response to DNA damage.
DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity.
Gekara et al., Umeå, Sweden. In Immunity, Mar 2015
Dysfunction in Ataxia-telangiectasia mutated (ATM), a central component of the DNA repair machinery, results in Ataxia Telangiectasia (AT), a cancer-prone disease with a variety of inflammatory manifestations.
Dysregulation of the DNA Damage Response and KMT2A Rearrangement in Fetal Liver Hematopoietic Cells.
Takagi et al., Tokyo, Japan. In Plos One, 2014
However, Kmt2a (Mll)-rearranged fusion mRNA was detected in Atm-knockout mice, which are defective in the DNA damage response, but not in wild-type mice.
Anthracyclines induce DNA damage response-mediated protection against severe sepsis.
Moita et al., Lisbon, Portugal. In Immunity, 2013
This salutary effect is strictly dependent on the activation of DNA damage response and autophagy pathways in the lung, as demonstrated by deletion of the ataxia telangiectasia mutated (Atm) or the autophagy-related protein 7 (Atg7) specifically in this organ.
Expression pattern of ataxia telangiectasia mutated (ATM), p53, Akt, and glycogen synthase kinase-3β in the striatum of rats treated with 3-nitropropionic acid.
Pelegrí et al., Barcelona, Spain. In J Neurosci Res, 2012
We examined whether cellular expression of ataxia telangiectasia mutated, p53, Akt, and glycogen synthase kinase-3beta, were involved in the striatal neurodegeneration in the brains of rats
Pathological neoangiogenesis depends on oxidative stress regulation by ATM.
Kubota et al., Tokyo, Japan. In Nat Med, 2012
The ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), acts as a barrier to cellular senescence and tumorigenesis.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
Bulavin et al., Singapore, Singapore. In Cell Metab, 2012
Here, we show that Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice; specifically, Wip1 deficiency prevents both conditions.
Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia.
Herrup et al., United States. In Nat Med, 2012
Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.
Cytoplasmic ATM protein kinase: an emerging therapeutic target for diabetes, cancer and neuronal degeneration.
Burn et al., Sioux Falls, United States. In Drug Discov Today, 2011
The gene mutated in this disease, Atm (A-T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein controlling cell-cycle progression.
Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.
Pearson et al., Dundee, United Kingdom. In Nat Genet, 2011
ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin
Mdm2 links genotoxic stress and metabolism to p53.
Li et al., Shanghai, China. In Protein Cell, 2010
Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related).
p53 control of bone remodeling.
Li et al., Shanghai, China. In J Cell Biochem, 2010
Moreover, Atm, c-Abl, and Mdm2, upstream regulators of p53 in DNA damage response, regulate osteoblast differentiation and bone remodeling as well.
ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation.
Camins et al., Barcelona, Spain. In J Cell Biochem, 2010
These data demonstrate how a new molecular network on ATM regulates the cell cycle through the control of pRb phosphorylation.
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage.
Frisan et al., Stockholm, Sweden. In Plos One, 2009
data demonstrate that MYC contributes to the activation of the ATM-dependent checkpoint responses, leading to cell death in response to specific genotoxic stimuli
The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1.
Chapple et al., London, United Kingdom. In Hum Mol Genet, 2009
Sacsin knockdown resulted in a reduction in cells expressing polyglutamine-expanded ataxin.
Rad3 and Sty1 function in Schizosaccharomyces pombe: an integrated response to DNA damage and environmental stress?
Sunnerhagen et al., Göteborg, Sweden. In Mol Microbiol, 2008
In Schizosaccharomyces pombe, the Ataxia Telangiectasia-mutated (Atm)/Atm and Rad 3 Related (Atr) homologue Rad3 is an essential regulator of the response to DNA damage and stalled replication forks.
ATM activation and DNA damage response.
Kozlov et al., Brisbane, Australia. In Cell Cycle, 2007
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and cellular phenotype of A-T that this gene would play a central role in the DNA damage response.
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